Many characteristics of peripheral neuropathies can be ascribed to a sensory defect. Electron microscopic and preliminary electrophysiological data suggest that in the toxic neuropathy resulting from acrylamide, the spinal cord terminations of muscle proprioceptive afferent fibers are functionally defective. Thus, spinal segmental and higher centers in the CNS do not receive appropriate information, contributing to neurological manifestations of ataxia, areflexia and motor incoordination. To investigate the extent and nature of the sensory defect in peripheral neuropathies, sensory neuropathies will be induced cats with doxorubicin (Adriamycin), an agent used for cancer therapy or with acrylamide, an industrial toxicological hazard, which can also produce, in its later stages, a mixed sensory-motor neuropathy. The spinal cord terminations of muscle spindles; the motoneurones (MN) and dorsal spinocerebellar tract cells (DSCT cells), will be investigated in neuropathic animals by physiological and histopathological means to determine: the nature of proprioceptive information they receive, how they perceive such information and what information they in turn provide to muscles and higher centers respectively. Evaluation of Mn function will provide a basis for understanding the areflexia common in neuropathies while determination of sensory information provided sensory-motor integrative centers will provide insight into the ataxia and motor incoordination. The use of two neuropathic agents will permit determination of the role of defective proprioception in both sensory and sensory-motor neuropathies.